CLINICAL PRESENTATION

Toxic Shock Syndrome (TSS)

Scalded Skin Syndrome
Ritters disease in newborn
food poisoning
PATHOBIOLOGY
Toxic Shock Syndrome: tampon use, trauma/surgery introduce bacteria bacteria colonize toxic shock syndrome
toxin-1 (TSST-1) released and diffuses systemically TSST-1 is a superantigen promotes excess cyto-
kines released (e.g., IL-1, TNF) acute fever, rash, desquamation on palms and soles, hypotensive shock
organ hypoperfusion and dysfunction possible death
Scalded Skin Syndrome: skin wound or cutting umbilicus in neonates promotes local epidermal infection exfolia-
tive toxins (e.g., ET-A,B) released and diffuse systemically epidermis separates and skin sloughs off
fluid loss and potential secondary infection possible death
food poisoning: bacteria release toxin in food such as custards heat-stable toxins (e.g., Enterotoxin SE-A)
ingested gastroenteritis self-limited, 8- to 24-hour nausea, vomiting, diarrhea, and abdominal pain
DIAGNOSIS
detection of toxin production by in vitro culture (blood cultures negative because organism does not invade bloodstream)
TREATMENT
removal of foreign bodies, drainage of purulent collections; fluid replacement; penicillinase-resistant penicillins hasten
recovery; (future) blocking effects of IL-1 and TNF with antibodies
QUICK FACTS
Antibiotics are not curativethey kill bacteria but do not remove already-released exotoxin.
Scalded skin syndrome has a 50% mortality rate among adults due to complications from hypovolemia and secondary
infection.
Ritters syndrome is the most severe form of scalded skin syndrome in neonates. It occurs after S. aureus colonizes the
cut umbilicus and releases ET-A,B systemically.
Staphylococcus aureus (toxin-mediated)
(TSS)
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